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Experimental studies on the nephrotoxicity of amphotericin B in ratsCentral Role of P2Y6 UDP Receptor in Arteriolar Myogenic ToneHypoxic pulmonary vasoconstriction requires connexin 40-mediated endothelial signal conduction.Selective deletion of Connexin 40 in renin-producing cells impairs renal baroreceptor function and is associated with arterial hypertension.Semiautomatic quantification of angiogenesis.Ischaemic heart disease in women: are there sex differences in pathophysiology and risk factors? Position paper from the working group on coronary pathophysiology and microcirculation of the European Society of CardiologyHigh flow conditions increase connexin43 expression in a rat arteriovenous and angioinductive loop modelPharmacological activation of KCa3.1/KCa2.3 channels produces endothelial hyperpolarization and lowers blood pressure in conscious dogsEndothelial mediators and communication through vascular gap junctions.Connexin 40 mediates the tubuloglomerular feedback contribution to renal blood flow autoregulationConnexins and gap junctions in the EDHF phenomenon and conducted vasomotor responses.Increased expression of cyclooxygenase 2 contributes to aberrant renin production in connexin 40-deficient kidneys.Dysfunctional nitric oxide signalling increases risk of myocardial infarction.Crucial importance of the endothelial K+ channel SK3 and connexin40 in arteriolar dilations during skeletal muscle contraction.Endothelial-specific deletion of connexin40 promotes atherosclerosis by increasing CD73-dependent leukocyte adhesion.Different pathways with distinct properties conduct dilations in the microcirculation in vivo.EDHF, but not NO or prostaglandins, is critical to evoke a conducted dilation upon ACh in hamster arterioles.Lack of vascular connexin 40 is associated with hypertension and irregular arteriolar vasomotion.Nitric oxide-induced decrease in calcium sensitivity of resistance arteries is attributable to activation of the myosin light chain phosphatase and antagonized by the RhoA/Rho kinase pathway.Angiotensin inhibition reduces glomerular damage and renal chemokine expression in MRL/lpr mice.Presentation, management, and outcomes of ischaemic heart disease in women.cGMP-dependent protein kinase mediates NO- but not acetylcholine-induced dilations in resistance vessels in vivo.Genetic deficit of SK3 and IK1 channels disrupts the endothelium-derived hyperpolarizing factor vasodilator pathway and causes hypertension.Prominent role of KCa3.1 in endothelium-derived hyperpolarizing factor-type dilations and conducted responses in the microcirculation in vivo.Substitution of connexin40 with connexin45 prevents hyperreninemia and attenuates hypertension.Intact endothelium-dependent dilation and conducted responses in resistance vessels of hypercholesterolemic mice in vivo.Myoendothelial coupling is not prominent in arterioles within the mouse cremaster microcirculation in vivo.Connexin45 cannot replace the function of connexin40 in conducting endothelium-dependent dilations along arterioles.Myoendothelial coupling through Cx40 contributes to EDH-induced vasodilation in murine renal arteries: evidence from experiments and modelling.Impaired endothelium-derived hyperpolarizing factor-mediated dilations and increased blood pressure in mice deficient of the intermediate-conductance Ca2+-activated K+ channel.A shear-dependent NO-cGMP-cGKI cascade in platelets acts as an auto-regulatory brake of thrombosisPublisher Correction: A shear-dependent NO-cGMP-cGKI cascade in platelets acts as an auto-regulatory brake of thrombosisEndothelium-specific replacement of the connexin43 coding region by a lacZ reporter geneDefective Cx40 maintains Cx37 expression but intact Cx40 is crucial for conducted dilations irrespective of hypertension
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P1053
A-5560-2009
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2000-01-01T00:00:00Z